Diarrhoea and dysentery are common enteric diseases which are fatal if they are not treated promptly. Dysentery caused by Shigella and other enteroinvasive pathogens like enteroinvasive Escherichia coli (EIEC) lead to high mortality and morbidity especially in children (WHO Report, 1986). Secondary complications such as haemolytic uraemic syndrome, colonic perforation are common. Of the enteropathogens Shigella is the most communicable; as few as ten organisms can cause dysentery in man. Enteroinvasive pathogens migrate to colonic epithelial cells, enter the colonic epithelial cells by inducing phagocytosis, multiply inside causing cell death and infect neighbouring cells (1). This results in tissue destruction, mucosal inflammation, epithelial ulceration and haemorrhage leading to the characteristic symptoms of dysentery, diarrhoea with blood and mucus.
The virulence of Shigella is not a very stable property. Mutants which are avirulent occur naturally and this can be achieved in laboratories simply by subculturing the virulent isolates (2). The virulent bacteria could be distinguished from avirulent bacteria by their ability to bind the dye, Congo red (CR) (3), to invade epithelial cells and to cause keratoconjunctivitis in guinea pig eye [Sereny test (2)]. Early studies employing classical genetics, identified a few major chromosomal loci (Purine, Xylose-Rhamnose, Glycerol kinase, Histidine and Maltose) as being responsible for expression of virulence in Shigella (4). However, only at the turn of this decade it became apparent that a large extra chromosomal genetic element (100-140 MDa) called megaplasmid is needed to code for the invasive phenotype of Shigella(5). It is clear that both chromosome and megaplasmid are necessary for the expression of total virulence (6) i.e. the ability to cause dysentery in man.
Detailed molecular genetic studies employing recombinant DNA techniques have led to the identification of several virulence related loci on the megaplasmid DNA. The virF locus confers the CR binding phenotype to the Shigella (7). The invasion plasmid antigen (ipa) genes B,C,D and A which encode polypeptides of 62 KDa, 42 KDa, 37 KDa and 78 KDa respectively are implicated in the invasion of the bacterium into colonic epithelial cells (8). Another locus virG is involved in conferring the ability to the bacterium to reinfect the neighbouring cells (9). The expression of these virulence genes is under thermoregulated factors (10). At 30.degree. C. Shigella is not virulent and virulence phenotypes are not expressed (11).